Laser direct overall water splitting for H2 and H2O2 production.

Hydrogen (H2) and hydrogen peroxide (H2O2) play crucial roles as energy carriers and raw materials for industrial production. However, the current techniques for H2 and H2O2 production rely on complex catalysts and involve multiple intermediate steps. In this study, we present a straightforward, environmentally friendly, and highly efficient laser-induced conversion method for overall water splitting to simultaneously generate H2 and H2O2 at ambient conditions without any catalysts. The laser direct overall water splitting approach achieves an impressive light-to-hydrogen energy conversion efficiency of 2.1%, with H2 production rates of 2.2 mmol/h and H2O2 production rates of 65 µM/h in a limited reaction area (1 mm2) within a short real reaction time (0.36 ms/h). Furthermore, we elucidate the underlying physics and chemistry behind the laser-induced water splitting to produce H2 and H2O2. The laser-induced cavitation bubbles create an optimal microenvironment for water-splitting reactions because of the transient high temperatures (104 K) surpassing the chemical barrier required. Additionally, their rapid cooling rate (1010 K/s) hinders reverse reactions and facilitates H2O2 retention. Finally, upon bubble collapse, H2 is released while H2O2 remains dissolved in the water. Moreover, a preliminary amplification experiment demonstrates the potential industrial applications of this laser chemistry. These findings highlight that laser-based production of H2 and H2O2 from water holds promise as a straightforward, environmentally friendly, and efficient approach on an industrial scale beyond conventional chemical catalysis.

Factor inhibiting HIF negatively regulates antiviral innate immunity via hydroxylation of IKKϵ.

Activation of type I interferon (IFN-1) signaling is essential to protect host cells from viral infection. The full spectrum of IFN-I induction requires the activation of a number of cellular factors, including IκB kinase epsilon (IKKϵ). However, the regulation of IKKϵ activation in response to viral infection remains largely unknown. Here, we show that factor inhibiting hypoxia-inducible factor (HIF) (FIH), an asparaginyl hydroxylase, interacts with IKKϵ and catalyzes asparagine hydroxylation of IKKϵ at Asn-254, Asn-700, and Asn-701, resulting in the suppression of IKKϵ activation. FIH-mediated hydroxylation of IKKϵ prevents IKKϵ binding to TBK1 and TRAF3 and attenuates the cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex-catalyzed K63-linked polyubiquitination of IKKϵ at Lys-416. In addition, Fih-deficient mice and zebrafish are more resistant to viral infection. This work uncovers a previously unrecognized role of FIH in suppressing IKKϵ activation for IFN signaling and antiviral immune responses.

Molecular characterization and expression analyses of five genes involved in the MyD88-dependent pathway of yellow catfish (Pelteobagrus fulvidraco) responding to challenge of Aeromonas hydrophila.

MyD88-dependent pathway mediated by Toll-like receptor is one of the vital ways activating immune responses. In order to identify the role of MyD88-dependent signaling pathway in yellow catfish, the Pf_MyD88, Pf_IRAK4, Pf_IRAK1, Pf_TRAF6 and Pf_NFκB1 (p105) (Pf: abbreviation of Pelteobagrus fulvidraco) were cloned and characterized respectively. The Pf_MyD88, Pf_IRAK4, Pf_IRAK1 and Pf_TRAF6 were all highly conserved among species and showed the highest homology to that of Pangasianodon hypophthalmus. Pf_NFκB1 showed the highest homology to that of Ictalurus punetaus. All of the five genes showed similar expression patterns in various tissues, with the highest expression level in the liver. These genes also showed similar expression levels in different embryonic development stages, except Pf_IRAK4. The higher expression level was detected from fertilized eggs to 1 day post hatching (dph), lower expression from 3 dph to 30 dph. After stimulation of inactivated Aeromonas hydrophila, the mRNA expressions of Pf_MyD88, Pf_IRAK4, Pf_IRAK1, Pf_TRAF6 and Pf_NFκB1 were significantly increased at 24 h in the liver, spleen, head kidney and trunk kidney, suggesting that all the five genes were involved in the innate immune response of yellow catfish. These results showed that MyD88-dependent signaling pathway plays important roles for disease defensing in the innate immune response. Meanwhile, inactivated A. hydrophila can cause strong innate immune response, which provides theoretical bases for the application of inactivated vaccines in defense against bacterial diseases of teleost.

Zebrafish mavs Is Essential for Antiviral Innate Immunity.

In mammals, the signaling adaptor mitochondrial antiviral signaling protein (MAVS) is a critical determinant in antiviral innate immunity. However, because of the lack of in vivo data, the physiological function of zebrafish mavs in response to viral infection is still not determined. In this study, we demonstrate that the long splicing isoform of zebrafish mavs promotes IFN regulatory factor 3 signaling and NF-κB signaling. Overexpression of this isoform of mavs enhances cellular antiviral responses. Disruption of mavs in zebrafish attenuates survival ratio on challenge with spring viremia of carp virus. Consistently, the antiviral-responsive genes and inflammatory genes are significantly reduced, and the replication of spring viremia of carp virus is increased in mavs-null zebrafish. Therefore, we provide in vivo evidence to support that zebrafish mavs is essential for antiviral innate immunity, similar to mammalian MAVS.

Transcriptomes of Zebrafish in Early Stages of Multiple Viral Invasions Reveal the Role of Sterols in Innate Immune Switch-On.

Although it is widely accepted that in the early stages of virus infection, fish pattern recognition receptors are the first to identify viruses and initiate innate immune responses, this process has never been thoroughly investigated. In this study, we infected larval zebrafish with four different viruses and analyzed whole-fish expression profiles from five groups of fish, including controls, at 10 h after infection. At this early stage of virus infection, 60.28% of the differentially expressed genes displayed the same expression pattern across all viruses, with the majority of immune-related genes downregulated and genes associated with protein synthesis and sterol synthesis upregulated. Furthermore, these protein synthesis- and sterol synthesis-related genes were strongly positively correlated in the expression pattern of the rare key upregulated immune genes, IRF3 and IRF7, which were not positively correlated with any known pattern recognition receptor gene. We hypothesize that viral infection triggered a large amount of protein synthesis that stressed the endoplasmic reticulum and the organism responded to this stress by suppressing the body's immune system while also mediating an increase in steroids. The increase in sterols then participates the activation of IRF3 and IRF7 and triggers the fish's innate immunological response to the virus infection.

Comparative Study on Immune Function of the Head and Trunk Kidney in Rainbow Trout Responding to IHNV Infection.

A teleost's kidney was divided into head kidney and trunk kidney. The head kidney is an important lymphatic organ, while the trunk kidney mainly performs osmotic pressure regulation and excretion functions. Previous studies have shown that the teleost's head kidney exerts a strong immune response against pathogen invasion, while the mechanism of immune response in the trunk kidney is still rarely reported. Therefore, in this study, we established an Infectious hematopoietic necrosis virus (IHNV) immersion infection model to compare the similarities and differences of immune response mechanisms between the head kidney and trunk kidney against viral infection. The results showed that IHNV infection causes severe tissue damage and inflammatory reaction in the head and trunk kidney, triggers a series of interferon cascade reactions, and produces strong immune response. In addition, the transcriptome data showed that the head kidney and trunk kidney had similar immune response mechanisms, which showed that the NOD-like receptor signaling pathway and Toll-like receptor signaling pathway were activated. In conclusion, despite functional differentiation, the teleost's trunk kidney still has a strong immune response, especially the interferon-stimulated genes, which have stronger immune response in the trunk kidney than in the head kidney when responding to IHNV infection. This study contributes to a more comprehensive understanding of the teleost immune system and enriches the theory of kidney immunity in teleosts.

First-principles investigation of in-plane anisotropies in XYTe4 monolayers with X = Hf, Zr, Ti and Y = Si, Ge.

In-plane anisotropic materials can introduce additional degrees of freedom while tuning their physical properties, which expand the range of opportunities for designing novel semiconductor devices and exploring distinct applications. In this work, we investigate the in-plane anisotropic electronic, elastic, transport and piezoelectric properties in a family of isostructural telluride XYTe4 (X = Hf, Zr and Ti, Y = Si and Ge) monolayers based on first-principles calculations. Six types of structures are verified to harbor direct bandgaps at the Γ point ranging between 0.98 and 1.36 eV. The orientation-dependent in-plane elastic stiffness of XYTe4 reveals the anisotropic and ultrasoft nature. Superior dielectric constants and giant switching effects are found in TiGeTe4 monolayers because of giant in-plane anisotropy. Strikingly, the piezoelectric coefficients of XSiTe4 differ by an order of magnitude along the two main directions. The strong in-plane anisotropic elastic properties of XYTe4 monolayers together with outstanding piezoelectric responses show that these structures can compete with that of transition metal dichalcogenides for applications in the field of flexible electronic devices.

Zebrafish sirt5 Negatively Regulates Antiviral Innate Immunity by Attenuating Phosphorylation and Ubiquitination of mavs.

The signaling adaptor MAVS is a critical determinant in retinoic acid-inducible gene 1-like receptor signaling, and its activation is tightly controlled by multiple mechanisms in response to viral infection, including phosphorylation and ubiquitination. In this article, we demonstrate that zebrafish sirt5, one of the sirtuin family proteins, negatively regulates mavs-mediated antiviral innate immunity. Sirt5 is induced by spring viremia of carp virus (SVCV) infection and binds to mavs, resulting in attenuating phosphorylation and ubiquitination of mavs. Disruption of sirt5 in zebrafish promotes survival ratio after challenge with SVCV. Consistently, the antiviral responsive genes are enhanced, and the replication of SVCV is diminished in sirt5-dificient zebrafish. Therefore, we reveal a function of zebrafish sirt5 in the negative regulation of antiviral innate immunity by targeting mavs.

Characterization, expression and function analysis of pfTLR5S and pfTLR5M in yellow catfish (Pelteobagrus fulvidraco) responding to bacterial challenge.

Toll-Like Receptors (TLRs) are important pattern recognition receptors, playing critical roles in the early innate immune response to defensing against pathogen invasion. In this study, we found both soluble form TLR5 (pfTLR5S) and membrane form TLR5 (pfTLR5M) in yellow catfish Pelteobagrus fulvidraco. The open reading frames (ORFs) of pfTLR5M and pfTLR5S genes were 2655 bp and 1947 bp in length, encoding 884 and 648 amino acids, respectively. pfTLR5M was composed of thirteen LRR domains, one TIR domain and one transmembrane domain. However, pfTLR5S have only fifteen LRR domains, without any TIR domain and transmembrane domain. Both pfTLR5M and pfTLR5S genes had the highest expression in liver, especially for pfTLR5S, which showed a noticeable high expression in liver. We also compared the relative mRNA expression levels of pfTLR5M and pfTLR5S in digestive and immune-related tissues after challenge of three different bacteria. In addition, we also found that pfTLR5S can interact with pfTLR5M, and inhibit the expression of pfTLR5M protein, while induced the expression of downstream proinflammatory factors, such as TNFα and IL8. These results revealed that both pfTLR5M and pfTLR5S play important and different roles in defensing against the invasion of flagellated bacteria, and they may function by binding to each other.

High-performance hierarchical O-SnS/I-ZnIn2S4 photodetectors by leveraging the synergy of optical regulation and band tailoring.

Low light absorption and limited carrier lifetime are critical obstacles inhibiting further performance improvement of 2D layered material (2DLM) based photodetectors, while scalable fabrication is an ongoing challenge prior to commercialization from the lab to market. Herein, wafer-scale SnS/ZIS hierarchical nanofilms, where out-of-plane SnS (O-SnS) is modified onto in-plane ZIS (I-ZIS), have been achieved by pulsed-laser deposition. The derived O-SnS/I-ZIS photodetector exhibits markedly boosted sensitivity as compared to a pristine ZIS device. The synergy of multiple functionalities contributes to the dramatic improvement, including the pronounced light-trapping effect of O-SnS by multiple scattering, the high-efficiency spatial separation of photogenerated electron-hole pairs by a type-II staggered band alignment and the promoted carrier transport enabled by the tailored electronic structure of ZIS. Of note, the unique architecture of O-SnS/I-ZIS can considerably expedite the carrier dynamics, where O-SnS promotes the electron transfer from SnS to ZIS whilst the I-ZIS enables high-speed electron circulation. In addition, the interlayer transition enables the bridging of the effective optical window to telecommunication wavelengths. Moreover, monolithic integration of arrayed devices with satisfactory device-to-device variability has been encompassed and a proof-of-concept imaging application is demonstrated. On the whole, this study depicts a fascinating functional coupling architecture toward implementing chip-scale integrated optoelectronics.

Opposing effects of deubiquitinase OTUD3 in innate immunity against RNA and DNA viruses.

Retinoic acid-inducible-I (RIG-I), melanoma differentiation-associated gene 5 (MDA5), and cyclic GMP-AMP synthase (cGAS) genes encode essential cytosolic receptors mediating antiviral immunity against viruses. Here, we show that OTUD3 has opposing role in response to RNA and DNA virus infection by removing distinct types of RIG-I/MDA5 and cGAS polyubiquitination. OTUD3 binds to RIG-I and MDA5 and removes K63-linked ubiquitination. This serves to reduce the binding of RIG-I and MDA5 to viral RNA and the downstream adaptor MAVS, leading to the suppression of the RNA virus-triggered innate antiviral responses. Meanwhile, OTUD3 associates with cGAS and targets at Lys279 to deubiquitinate K48-linked ubiquitination, resulting in the enhancement of cGAS protein stability and DNA-binding ability. As a result, Otud3-deficient mice and zebrafish are more resistant to RNA virus infection but are more susceptible to DNA virus infection. These findings demonstrate that OTUD3 limits RNA virus-triggered innate immunity but promotes DNA virus-triggered innate immunity.

OTUB1 augments hypoxia signaling via its non-canonical ubiquitination inhibition of HIF-1α during hypoxia adaptation.

As a main regulator of cellular responses to hypoxia, the protein stability of hypoxia-inducible factor (HIF)-1α is strictly controlled by oxygen tension dependent of PHDs-catalyzed protein hydroxylation and pVHL complex-mediated proteasomal degradation. Whether HIF-1α protein stability as well as its activity can be further regulated under hypoxia is not well understood. In this study, we found that OTUB1 augments hypoxia signaling independent of PHDs/VHL and FIH. OTUB1 binds to HIF-1α and depletion of OTUB1 reduces endogenous HIF-1α protein under hypoxia. In addition, OTUB1 inhibits K48-linked polyubiquitination of HIF-1α via its non-canonical inhibition of ubiquitination activity. Furthermore, OTUB1 promotes hypoxia-induced glycolytic reprogramming for cellular metabolic adaptation. These findings define a novel regulation of HIF-1α under hypoxia and demonstrate that OTUB1-mediated HIF-1α stabilization positively regulates HIF-1α transcriptional activity and benefits cellular hypoxia adaptation.

Molecular characteristics, polymorphism and expression analysis of mhc â ¡ in yellow catfish(pelteobagrus fulvidraco)responding to Flavobacterium columnare infection.

The major histocompatibility complex (MHC) is an important component of the immune system of vertebrates, which plays a vital role in presenting extrinsic antigens. In this study, we cloned and characterized the mhc ⅡA and mhc ⅡB genes of yellow catfish Pelteobagrus fulvidraco. The open reading frames (ORFs) of mhc ⅡA and mhc ⅡB genes were 708 bp and 747bp in length, encoding 235 and 248 amino acids, respectively. The structure of mhc ⅡA and mhc ⅡB includes a signal peptide, an α1/ß1 domain, an α2/ß2 domain, a transmembrane region and a cytoplasmic region. Homologous identity analysis revealed that both mhc ⅡA and mhc ⅡB shared high protein sequence similarity with that of Chinese longsnout catfish Leiocassis longirostris. mhc ⅡA and mhc ⅡB showed similar expression patterns in different tissues, with the higher expression level in spleen, head kidney and gill and lower expression in liver, stomach, gall bladder and heart. The mRNA expression level of mhc ⅡA and mhc ⅡB in different embryonic development stages also showed the similar trends. The higher expression was detected from fertilized egg to 32 cell stage, low expression from multicellular period to 3 days post hatching (dph), and then the expression increased to a higher level from 4 dph to 14 dph. The mRNA expression levels of mhc ⅡA and mhc ⅡB were significantly up-regulated not only in the body kidney and spleen, but also in the midgut, hindgut, liver and gill after challenge of Flavobacterium columnare. The results suggest that Mhc Ⅱ plays an important role in the anti-infection process of yellow catfish P. fulvidraco.

EGLN1 prolyl hydroxylation of hypoxia-induced transcription factor HIF1α is repressed by SET7-catalyzed lysine methylation.

Egg-laying defective nine 1 (EGLN1) functions as an oxygen sensor to catalyze prolyl hydroxylation of the transcription factor hypoxia-inducible factor-1 α under normoxia conditions, leading to its proteasomal degradation. Thus, EGLN1 plays a central role in the hypoxia-inducible factor-mediated hypoxia signaling pathway; however, the posttranslational modifications that control EGLN1 function remain largely unknown. Here, we identified that a lysine monomethylase, SET7, catalyzes EGLN1 methylation on lysine 297, resulting in the repression of EGLN1 activity in catalyzing prolyl hydroxylation of hypoxia-inducible factor-1 α. Notably, we demonstrate that the methylation mimic mutant of EGLN1 loses the capability to suppress the hypoxia signaling pathway, leading to the enhancement of cell proliferation and the oxygen consumption rate. Collectively, our data identify a novel modification of EGLN1 that is critical for inhibiting its enzymatic activity and which may benefit cellular adaptation to conditions of hypoxia.

Repression of p53 function by SIRT5-mediated desuccinylation at Lysine 120 in response to DNA damage.

p53 is a classic tumor suppressor that functions in maintaining genome stability by inducing either cell arrest for damage repair or cell apoptosis to eliminate damaged cells in response to different types of stress. Posttranslational modifications (PTMs) of p53 are thought to be the most effective way for modulating of p53 activation. Here, we show that SIRT5 interacts with p53 and suppresses its transcriptional activity. Using mass spectrometric analysis, we identify a previously unknown PTM of p53, namely, succinylation of p53 at Lysine 120 (K120). SIRT5 mediates desuccinylation of p53 at K120, resulting in the suppression of p53 activation. Moreover, using double knockout mice (p53-/-Sirt5-/-), we validate that the suppression of p53 target gene expression and cell apoptosis upon DNA damage is dependent on cellular p53. Our study identifies a novel PTM of p53 that regulates its activation as well as reveals a new target of SIRT5 acting as a desuccinylase.

Zebrafish sirt7 Negatively Regulates Antiviral Responses by Attenuating Phosphorylation of irf3 and irf7 Independent of Its Enzymatic Activity.

Sirt7 is one member of the sirtuin family proteins with NAD (NAD+)-dependent histone deacetylase activity. In this study, we report that zebrafish sirt7 is induced upon viral infection, and overexpression of sirt7 suppresses cellular antiviral responses. Disruption of sirt7 in zebrafish increases the survival rate upon spring viremia of carp virus infection. Further assays indicate that sirt7 interacts with irf3 and irf7 and attenuates phosphorylation of irf3 and irf7 by preventing tbk1 binding to irf3 and irf7. In addition, the enzymatic activity of sirt7 is not required for sirt7 to repress IFN-1 activation. To our knowledge, this study provides novel insights into sirt7 function and sheds new light on the regulation of irf3 and irf7 by attenuating phosphorylation.

Spontaneous flexoelectricity and band engineering in MS2 (M = Mo, W) nanotubes.

Spontaneous flexoelectricity in transition metal dichalcogenide (TMD) nanotubes is critical to the design of new energy devices. However, the electronic properties adjusted by the flexoelectric effect in TMD nanotubes remain vague. In this work, we investigate the effect of flexoelectricity on band engineering in single- and double-wall MS2 (M = Mo, W) nanotubes with different diameters based on first-principles calculations and an atomic-bond-relaxation method. We find that the energy bandgap reduces and the polarization and flexoelectric voltage increase with decreasing diameter of single-wall MS2 nanotubes. The polarization charges promoted by the flexoelectric effect can lead to a straddling-to-staggered bandgap transition in the double-wall MS2 nanotubes. The critical diameters for bandgap transition are about 3.1 and 3.6 nm for double-wall MoS2 and WS2 nanotubes, respectively, which is independent of chirality. Our results provide guidance for the design of new energy devices based on spontaneous flexoelectricity.